From Beyond The Rainbow Somewhere

Day: 11/06/2013

Post navigation

The meteor that exploded over Chelyabinsk, Russia in February 2013 was “a wake-up call,” according to a University of California, Davis scientist who participated in analyzing the event. The work is published November 7, 2013 in the journal Science by an international team of researchers. “If humanity does not want to go the way of the dinosaurs, we need to study an event like this in detail,” said Qing-Zhu Yin, professor in the Department of Earth and Planetary Sciences at UC Davis.

Chelyabinsk was the largest meteoroid strike since the Tunguska event of 1908, and thanks to modern technology from consumer video cameras to advanced laboratory techniques, provides an unprecedented opportunity to study such an event, the authors note.

The Chelyabinsk meteorite belongs to the most common type of meteorite, an “ordinary chondrite.” If a catastrophic meteorite strike were to occur in the future, it would most likely be an object of this type, Yin said.

The team was led by Olga Popova of the Russian Academy of Sciences in Moscow, and by NASA Ames and SETI Institute meteor astronomer Peter Jenniskens, and included 57 other researchers from nine countries.

“Our goal was to understand all circumstances that resulted in the damaging shock wave that sent over 1200 people to hospitals in the Chelyabinsk Oblast area that day,” said Jenniskens. The explosion was equivalent to about 600 thousand tons of TNT, 150 times bigger than the 2012 Sutter’s Mill meteorite in California.

Based on viewing angles from videos of the fireball, the team calculated that the meteoroid entered Earth’s atmosphere at just over 19 kilometers per second, slightly faster than had previously been reported.

“Our meteoroid entry modeling showed that the impact was caused by a 20-meter sized single chunk of rock that efficiently fragmented at 30 km altitude,” Popova said. (A meteoroid is the original object; a meteor is the “shooting star” in the sky; and a meteorite is the object that reaches the ground.)

The meteor’s brightness peaked at an altitude of 29.7 km (18.5 miles) as the object exploded. For nearby observers it briefly appeared brighter than the Sun and caused some severe sunburns.

The team estimated that about three-quarters of the meteoroid evaporated at that point. Most of the rest converted to dust and only a small fraction (4,000 to 6,000 kilograms, or less than 0.05 percent) fell to the ground as meteorites. The dust cloud was so hot it glowed orange.

The largest single piece, weighing about 650 kilograms, was recovered from the bed of Lake Chebarkul in October by a team from Ural Federal University led by Professor Viktor Grokhovsky.

Shockwaves from the airburst broke windows, rattled buildings and even knocked people from their feet. Popova and Jenniskens visited over 50 villages in the area and found that the shockwave caused damage about 90 kilometers (50 miles) on either side of the trajectory. The team showed that the shape of the damaged area could be explained from the fact that the energy was deposited over a range of altitudes.

The object broke up 30 kilometers up under the enormous stress of entering the atmosphere at high speed. The breakup was likely facilitated by abundant “shock veins” that pass through the rock, caused by an impact that occurred hundreds of millions of years ago. These veins would have weakened the original meteoroid.

Yin’s laboratory at UC Davis carried out chemical and isotopic analysis of the meteorites. Professor Ken Verosub, also of the Department of Earth and Planetary Sciences, measured the magnetic properties of metallic grains in the meteorite. Doug Rowland, project scientist in the Center for Molecular and Genomic Imaging at the UC Davis Department of Biomedical Engineering, contributed X-ray computed tomography (CT) scanning of the rock.

Put together, these measurements confirmed that the Chelyabinsk object was an ordinary chondrite, 4,452 million years old, and that it last went through a significant shock event about 115 million years after the formation of the solar system 4,567 million years ago. That impact was at a much later date than in other known chondrites of the same type, Yin said, suggesting a violent history.

Jenniskens calculated that the object may have come from the Flora asteroid family in the asteroid belt, but the chunk that hit the Chelyabinsk area was apparently not broken up in the asteroid belt itself. Researchers at the University of Tokyo and Waseda University in Japan found that the rock had been exposed to cosmic rays for only about 1.2 million years, unusually short for rocks originating in the Flora family.

Jenniskens speculates that Chelyabinsk belonged to a bigger “rubble pile” asteroid that broke apart 1.2 million years ago, possibly in an earlier close encounter with Earth.

The rest of that rubble could still be around as part of the near-earth asteroid population, Jenniskens said.

Yin noted that major meteorite strikes like Tunguska or Chelyabinsk occur more frequently than we tend to think. For example, four tons of material were recovered from a meteor shower in Jilin, China in 1976.

“Chelyabinsk serves as unique calibration point for high energy meteorite impact events for our future studies,” he said. Technology for early detection of these objects is needed, Yin said—such as the Large Synoptic Survey Telescope, currently being developed by an international team headed by UC Davis physics professor J. Anthony Tyson.

New research on pond snails has revealed that high levels of stress can block memory processes. Researchers from the University of Exeter and the University of Calgary trained snails and found that when they were exposed to multiple stressful events they were unable remember what they had learned. Previous research has shown that stress also affects human ability to remember. This study, published in the journal PLOS ONE, found that experiencing multiple stressful events simultaneously has a cumulative detrimental effect on memory.

Dr Sarah Dalesman, a Leverhulme Trust Early Career Fellow, from the University of Exeter, formally at the University of Calgary, said: “It’s really important to study how different forms of stress interact as this is what animals, including people, frequently experience in real life. By training snails, and then observing their behaviour and brain activity following exposure to stressful situations, we found that a single stressful event resulted in some impairment of memory but multiple stressful events prevented any memories from being formed.”

The pond snail, Lymnaea stagnalis, has easily observable behaviours linked to memory and large neurons in the brain, both useful benefits when studying memory processes. They also respond to stressful events in a similar way to mammals, making them a useful model species to study learning and memory.

In the study, the pond snails were trained to reduce how often they breathed outside water. Usually pond snails breathe underwater and absorb oxygen through their skin. In water with low oxygen levels the snails emerge and inhale air using a basic lung opened to the air via a breathing hole.

To train the snails not to breathe air they were placed in poorly oxygenated water and their breathing holes were gently poked every time they emerged to breathe. Snail memory was tested by observing how many times the snails attempted to breathe air after they had received their training. Memory was considered to be present if there was a reduction in the number of times they opened their breathing holes. The researchers also assessed memory by monitoring neural activity in the brain.

Immediately before training, the snails were exposed to two different stressful experiences, low calcium – which is stressful as calcium is necessary for healthy shells – and overcrowding by other pond snails.

When faced with the stressors individually, the pond snails had reduced ability to form long term memory, but were still able to learn and form short and intermediate term memory lasting from a few minutes to hours. However, when both stressors were experienced at the same time, results showed that they had additive effects on the snails‘ ability to form memory and all learning and memory processes were blocked.

An infant can recognise a lullaby heard in the womb for several months after birth, potentially supporting later speech development. This is indicated in a new study at the University of Helsinki.

The study focused on 24 women during the final trimester of their pregnancies. Half of the women played the melody of Twinkle Twinkle Little Star to their fetuses five days a week for the final stages of their pregnancies. The brains of the babies who heard the melody in utero reacted more strongly to the familiar melody both immediately and four months after birth when compared with the control group. These results show that fetuses can recognise and remember sounds from the outside world.

This is significant for the early rehabilitation, since rehabilitation aims at long-term changes in the brain.

“Even though our earlier research indicated that fetuses could learn minor details of speech, we did not know how long they could retain the information. These results show that babies are capable of learning at a very young age, and that the effects of the learning remain apparent in the brain for a long time,” expounds Eino Partanen, who is currently finishing his dissertation at the Cognitive Brain Research Unit.

“This is the first study to track how long fetal memories remain in the brain. The results are significant, as studying the responses in the brain let us focus on the foundations of fetal memory. The early mechanisms of memory are currently unknown,” points out Dr Minna Huotilainen, principal investigator.

The researchers believe that song and speech are most beneficial for the fetus in terms of speech development. According to the current understanding, the processing of singing and speech in the babies brains are partly based on shared mechanisms, and so hearing a song can support a baby’s speech development. However, little is known about the possible detrimental effects that noise in the workplace can cause to a fetus during the final trimester. An extensive research project on this topic is underway at the Finnish Institute of Occupational Health.

The study was published by the esteemed American scientific journal PLoS ONE. The research was conducted at the Academy of Finland’s Finnish Centre of Excellence in Interdisciplinary Music Research as well as the Cognitive Brain Research Unit at the University of Helsinki Institute of Behavioural Sciences.

Scientists have discovered a new ligament in the human knee, which seems to play an important role in patients who suffer ligament injuries and their knees continue to ‘give way’ even after treatment.

The discovery was made by orthopaedic surgeons Dr Steven Claes and Professor Dr Johan Bellemans of the University Hospitals Leuven, who have been conducting research for the last four years into serious anterior cruciate ligament (ACL) injuries.

They studied 41 cadaveric knees using macroscopic dissection techniques to examine why some patients continue to suffer the pivot shift, where the knee gives way during physical activity.

ACL tears are common among athletes and those who play sports such as basketball and football.

Dr Claes and Dr Bellemans followed on from the work of French surgeon Paul Ferdinand Segon in 1879, who penned an article that suggested an additional ligament may exist on the anterior of the knee.

Orthopedic surgeons find a new ligament that may explain why knees ‘give

Their research, published in the Journal of Anatomy, shows the new ligament now known as the anterolateral ligament (ALL) was present in all but one of the 41 knees.

Subsequent research shows that pivot shift of the knee in patients with an ACL tear is caused by an injury in the ALL ligament.

The study concluded: “Given its structure and anatomic location, the ALL is hypothesized to control internal tibial rotation and thus to affect the pivot shift phenomenon, although further studies are needed to investigate its biomechanical function.”

Dr Claes and Professor Bellemans are currently working on a surgical technique to correct ALL injuries, which could be ready within the next seven years.

There are many voices in the operating theatre, and sometimes the most important are those that don’t use words at all.

For a newcomer, the operating theatre is an overwhelming place. Sound is all around: beeps, alarms, the noise of people moving. Speech, when it surfaces, uses an alien language peppered with abbreviations and jargon. Photograph: Sean Smith/Guardian

The first time I took part in an operation I had no idea what was going on. As a new medical student I hadn’t learned the language of surgery. I didn’t even know there was a language of surgery. A few years later, as a surgeon myself, this language had become second nature and I didn’t even know I was using it.

Of course there are many voices in the operating theatre. They don’t always say what they mean or mean what they say. And sometimes the most important voices are those that don’t use words at all.

For several years I’ve been leading research projects that investigate how people communicate during surgery. At Medicine Unboxed in Cheltenham, I’m going to explore how to read some of these surgical voices and make sense of what they say.

Of course the story starts with the patient. What happens to their voice during surgery? At first glance, it seems to have disappeared altogether, especially if the operation needs a general anaesthetic. In the anaesthetic room the patient gradually relinquishes autonomy, leaving behind their personhood and their power to speak for themselves as powerful drugs make them unconscious.

But they haven’t stopped communicating. Speech mutates into a language of the unconscious body. Functions that we take for granted and scarcely notice – our heart beating, our lungs breathing, our blood circulating – are represented by wavy lines on a screen or the beep of a machine. Words have turned into traces, and the voice of the anaesthetised patient has become transformed.

Throughout the operation the surgical team monitors this wordless commentary, this constant unconscious broadcast of the body. Any variation – a change in rhythm, a subtle inflection of pitch – will put the team on high alert. The team has become fluent in the language of unconsciousness.

When the operation is over, when the wound is closed and the dressings are in place, the anaesthetist disconnects these machines and hands back the power of speech.

Reading voices

In the operating theatre, different voices are in play. At the centre is the scrub team – those who operate on the body itself. Around them are other members of the group – equally important but differently so – and all have different voices.

The surgeon’s voice is often muted, soft, muffled by a mask. Intended for the scrub team only, it may be inaudible beyond. Voices spread out in ripples from the scrub team: requests for instruments, instructions to others in the theatre. The anaesthetist, the operating department practitioner, the runner nurse – all have their ways of speaking, their vocabularies, their own vocal fingerprint.

The voices you hear depend on where you’re standing. Like conversation at a party, there are ebbs and flows, natural rhythms and patterns. Often you can’t make out the words, but you have to interpret the many meanings within this soundscape of surgery and recognise when they involve you. You develop new sensitivities, new ways of reading what is said.

What do these voices convey? Some are the voices of people talking in ordinary words. But others are different. Some are distorted voices, pulled out of shape by their peculiar setting. Some are transformed voices, expressed through machines instead of words. And some are silent voices, conveying their message by what they do not say.

Reading voices isn’t easy. For a newcomer, the operating theatre is an overwhelming place. Sound is all around: beeps, alarms, the noise of people moving. Sometimes music. And speech, when it surfaces, uses an alien language, peppered with abbreviations and jargon.

Once you get used to it, you can tell how things are going the instant you step in. If all is well, there’s a general buzz of conversation, movement, activity. But if things are going badly, you sense the tension without even knowing how. The most eloquent voice of all is the voice of silence: the voice that says ‘we’ve got a problem here and we all need to focus on fixing it’.

In my conversation at Medicine Unboxed, I hope to unpick some of these ideas, exploring what’s different about surgical voices and what they can and cannot say.

But while the overall evidence on routine screening is insufficient, clinicians should remain alert to early signs or symptoms of cognitive impairment and evaluate accordingly, the USPSTF said in a statement.

The draft recommendation applies to adults over age 65 years without signs or symptoms of cognitive impairment. It will be posted on the USPSTF Web site and be open for public comment before the Task Force develops a final recommendation.

This recommendation updates the 2003 USPSTF statement that also concluded that the evidence was insufficient to recommend for or against routine screening for dementia. Unlike that earlier recommendation, this updated version considered the evidence on screening for and treatment of mild cognitive impairment in addition to dementia, and on how screening affects decision-making and planning.

Brief Screening Tools

With new data on screening accuracy, the Task Force was able to conclude that there is adequate information on the accuracy of some brief screening tools to identify dementia. The most widely studied instrument is the Mini-Mental State Examination. For the most commonly reported cut points (23/24 or 24/25), the pooled sensitivity from 14 studies was 88.3% (95% confidence interval [CI], 81.3% – 92.9%) and specificity was 86.2% (95% CI, 81.8% – 89.7%).

Other screening tools include the Clock Draw Test, Mini-Cog, Memory Impairment Screen, Abbreviated Mental Test, Short Portable Mental Status Questionnaire, Free and Cued Selective Reminding Test, 7-Minute Screen, Telephone Interview for Cognitive Status, and Informant Questionnaire on Cognitive Decline in the Elderly. These tests have reasonable test performance according to some studies, but their sensitivity or specificity ranged widely and optimal diagnostic cut-points for many are unclear, the statement said.

The new data suggest that treatment of mild to moderate dementia with acetylcholinesterase inhibitors (AChEIs) and memantine, and with nonpharmacologic interventions, such as cognitive stimulation and exercise, results in small improvement in cognitive function, and that interventions aimed at caregivers result in reduced caregiver burden and depression. However, the clinical significance of these improvements is uncertain, according to the Task Force report.

No published evidence was found on the effect of screening on decision-making or planning by patients, clinicians, or caregivers, the Task Force concluded.

Critical Gap

“This is a critical gap in the evidence, and more research is needed so we can better understand the benefits and risks of screening and understand the impact early detection can have on the lives of patients and their families,” commented Task Force member Douglas K. Owens, MD, in press materials accompanying the draft document.

More data will be required before such screening could be recommended. “If we had information on treatments that might be available in early dementia that were highly effective, I think that would be one thing,” Task Force co-vice chair Albert Siu, MD, toldMedscape Medical News. “And, if we found interventions that would be effective in terms of helping individuals with early dementia and their family members to make decisions and plan, we would consider that to be important evidence.”

The Task Force also determined that there is inadequate evidence on nonpharmacologic interventions and on the harms of screening (eg, the impact of labeling and of false-positive results). There is, however, evidence that AChEIs are associated with adverse events, some of which are serious, for example, central nervous system disturbances and arrhythmia.

“Overall, the USPSTF was unable to estimate the balance of benefits and harms of screening for cognitive impairment,” the draft recommendation statement concludes.

The Task Force noted that no professional organization has formal guidelines on screening for dementia or cognitive impairment. However, earlier this year, the Alzheimer’s Associationpublished guidanceon the detection of cognitive impairment during the Annual Wellness Visit and recommended an algorithm starting with a health risk assessment, patient observation, and unstructured questioning. Use of a brief structured assessment is recommended if signs or symptoms of cognitive impairment are present or if an informant is unavailable to confirm the absence of signs or symptoms.

Dr. Siu noted that dementia screening for patients showing signs and symptoms of dementia was beyond the scope of the Task Force review. “The scope was what do you do on a population basis for individuals who are not complaining of any symptoms and there have been no signs,” he said. “The question is, should you be automatically screening these people? Certainly, if someone comes in with signs or symptoms, that requires evaluation.”

Dementia affects up to about 5.5 million Americans. Its prevalence increases with age, affecting 5% in those aged 71 to 79 years, 24% in those aged 80 to 89 years, and 37% in those older than age 90 years.

The estimated total health, long-term care, and hospice care costs for dementia in the United States were $183 billion in 2011. These costs don’t include the estimated $202 billion in uncompensated care that informal caregivers provide annually.

“Dementia is a very serious issue that has a significant impact on the lives of older adults and their families,” said Dr. Siu in the press statement. “Although the benefits and harms of what we can offer patients through routine screening are unclear right now, clinicians should remain alert to early signs or symptoms of cognitive impairment and evaluate their patients as appropriate.”

The Task Force is now providing an opportunity for public comment on the draft recommendation until December 2. All public comments will then be considered as the Task Force develops its final recommendation. Dr. Siu expects a final recommendation in the spring of 2014.

“Regardless of what our recommendation is, it will serve as guidance to physicians,” rather than a directive, Dr. Siu toldMedscape Medical News.

The Task Force is an independent, volunteer panel of national experts in prevention and evidence-based medicine that works to improve the health of all Americans by making evidence-based recommendations about clinical preventive services, such as screenings, counseling services, and preventive medications.

Carbon science is a field of intense research. Not only does carbon form the chemical basis of life, but it has rich chemistry and physics, making it a target of interest to material scientists. From graphite to diamond to Buckminster fullerenes, nanotubes and graphene, carbon can display in a range of structures.

But the search for a stable three-dimensional form of carbon that is metallic underambient conditions, including temperature and pressure, has remained an ongoing challenge for scientists in the field.

“The interlocking of hexagons provides two unique features – hexagonal arrangement introduces metallic character, and the interlocking form with tetrahedral bonding guarantees stability,” said co-lead investigator Puru Jena, Ph.D., distinguished professor of physics in the VCU College of Humanities and Sciences.

The right combination of these properties could one day be applied to a variety of technologies.

“Unlike high-pressure techniques that require three terapascals of pressure to make carbon metallic, the studied structures are stable at ambient conditions and may be synthesized using benzene or polyacenes molecules,” said co-lead investigator Qian Wang, Ph.D., who holds a professor position at Peking University and an adjunct faculty position at VCU.

“The new metalliccarbonstructures may have important applications in lightweight metals for space applications, catalysis and in devices showing negative differential resistance or superconductivity,” Wang said.

According to Jena, the team is still early in its discovery process, but hope that these findings may move the work from theory to the experimental phase.

Whitehead Institute scientists report that the gene mutated in the rare hereditary disorder known as Birt-Hogg-Dubé cancer syndrome also prevents activation of mTORC1, a critical nutrient-sensing and growth-regulating cellular pathway.

This is an unexpected finding, as some cancers keep this pathway turned on to fuel their unchecked growth and expansion. In the case of Birt-Hogg-Dubé syndrome, the mutated gene prevents mTORC1 pathway activation early in the formation of tumors. Reconciling these opposing roles may give scientists a new perspective on how cancer cells can distort normal cellular functions to maintain their own harmful ways.

Cells use the mTORC1 (for “mechanistic target of rapamycin complex 1”) pathway to regulate growth in response to the availability of certain nutrients, including amino acids. Whitehead Member David Sabatini and other researchers have teased apart many components of this pathway, but the precise mechanism by which nutrient levels are actually sensed has remained elusive. Recently, Sabatini and his lab determined that a family of proteins known as Rag GTPases act as a switch for the pathway—when nutrients are present, the Rag proteins turn on the mTORC1 pathway.

Now, several members of the Sabatini lab, including graduate student Zhi-Yang Tsun, have determined that the FLCN protein acts as a trigger to activate the Rag protein switch. Their work is described in the November 7 issue of the journalMolecular Cell.

“Zhi has ascribed a molecular function to this protein, and that’s a major contribution,” says Sabatini, who is also a Howard Hughes Medical Institute investigator and a professor of biology at MIT. “For the first time, we have a biochemical function that’s associated with it. And in my view, that’s an important first step to understanding how it might be involved in cancer.”

Before Tsun’s work, very little was known about FLCN’s role in the cell. In the early 2000s, scientists determined that mutations in the gene coding for FLCN caused the rare cancer Birt-Hogg-Dubé syndrome, but the syndrome’s symptoms offered little insight into FLCN’s molecular function.

Birt-Hogg-Dubé syndrome causes unsightly but benign hair follicle tumors on the face, benign tumors in the lungs that can lead to collapsed lungs, and kidney cancer. The syndrome is an autosomal dominant disorder, which means that a child inheriting one mutated copy of the FLCN gene will eventually develop the syndrome. Currently, the disease is managed by treating symptoms, but no cure exists.

FLCN’s dual roles—as a cause of a rare cancer in its mutated form and as a trigger for a growth pathway that is often hijacked in cancer cells—has prompted Tsun and Sabatini to rethink how a mutation can push cells to become cancerous.

“Basically, the mTORC1 pathway is essential for life,” explains Tsun. “So when you lose this nutrient switch or if it can’t be turned on, then the cell seems to freak out and cause all other growth promoting pathways to be turned on to somehow overcompensate for this loss. And this is actually what we see in patient tumors.”

For Birt-Hogg-Dubé syndrome patients and their families, better understanding of FCLN’s function moves the field one step closer to developing a therapy.

“Usually diseases are first described, then the responsible gene or genes are identified, and then that gene’s molecular function is figured out,” says Tsun. “And you need to know the gene’s function before you can start working on drugs or therapy. We’ve done that third step, which is a very important discovery for these patients.”

We physicians with all our training, knowledge and authority often acquire a rather large ego that tends to make it difficult to admit we are wrong. So, here it is. I freely admit to being wrong.. As a heart surgeon with 25 years experience, having performed over 5,000 open-heart surgeries,today is my day to right the wrong with medical and scientific fact. I trained for many years with other prominent physicians labelled “opinion makers.” Bombarded with scientific literature, continually attending education seminars, we opinion makers insisted heart disease resulted from the simple fact of elevated blood cholesterol. The only accepted therapy was prescribing medications to lower cholesterol and a diet that severely restricted fat intake. The latter of course we insisted would lower cholesterol and heart disease. Deviations from these recommendations were considered heresy and could quite possibly result in malpractice.

These recommendations are no longer scientifically or morally defensible. The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated. The long-established dietary recommendations have created epidemics of obesity and diabetes, the consequences of which dwarf any historical plague in terms of mortality, human suffering and dire economic consequences. Despite the fact that 25% of the population takes expensive statin medications and despite the fact we have reduced the fat content of our diets, more Americans will die this year of heart disease than ever before. Statistics from the American Heart Association show that 75 million Americans currently suffer from heart disease, 20 million have diabetes and 57 million have pre-diabetes. These disorders are affecting younger and younger people in greater numbers every year. Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped. Inflammation is not complicated — it is quite simply your body’s natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process,a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial. What thoughtful person would willfully expose himself repeatedly to foods or other substances that are known to cause injury to the body? Well,smokers perhaps, but at least they made that choice willfully. The rest of us have simply followed the recommended mainstream dietthat is low in fat and high in polyunsaturated fats and carbohydrates, not knowing we were causing repeated injury to our blood vessels. This repeated injury creates chronic inflammation leading to heart disease, stroke, diabetes and obesity. Let me repeat that: The injury and inflammation in our blood vessels is caused by the low fat diet recommended for years by mainstream medicine. What are the biggest culprits of chronic inflammation? Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, flour and all the products made from them) and the excess consumption of omega-6 vegetable oils like soybean, corn and sunflower that are found in many processed foods. Take a moment to visualize rubbing a stiff brush repeatedly over soft skin until it becomes quite red and nearly bleeding. you kept this up several times a day, every day for five years. If you could tolerate this painful brushing, you would have a bleeding, swollen infected area that became worse with each repeated injury. This is a good way to visualize the inflammatory process that could be going on in your body right now. Regardless of where the inflammatory process occurs, externally or internally, it is the same. I have peered inside thousands upon thousands of arteries. A diseased artery looks as if someone took a brush and scrubbed repeatedly against its wall. Several times a day, every day, the foods we eat create small injuries compounding into more injuries, causing the body to respond continuously and appropriately with inflammation. While we savor the tantalizing taste of a sweet roll, our bodies respond alarmingly as if a foreign invader arrived declaring war. Foods loaded with sugars and simple carbohydrates, or processed withomega-6 oils for long shelf life have been the mainstay of the American diet for six decades. These foods have been slowly poisoning everyone. How does eating a simple sweet roll create a cascade of inflammation to make you sick? Imagine spilling syrup on your keyboard and you have a visual of what occurs inside the cell. When we consume simple carbohydrates such as sugar, blood sugar rises rapidly. In response, your pancreas secretes insulin whose primary purpose is to drive sugar into each cell where it is stored for energy. If the cell is full and does not need glucose, it is rejected to avoid extra sugar gumming up the works. When your full cells reject the extra glucose, blood sugar rises producing more insulin and the glucose converts to stored fat. What does all this have to do with inflammation? Blood sugar is controlled in a very narrow range. Extra sugar molecules attach to a variety of proteins that in turn injure the blood vessel wall. This repeated injury to the blood vessel wall sets off inflammation. When you spike your blood sugar level several times a day, every day, it is exactly like taking sandpaper to the inside of your delicate blood vessels. While you may not be able to see it, rest assured it is there. I saw it in over 5,000 surgical patients spanning 25 years who all shared one common denominator — inflammation in their arteries. Let’s get back to the sweet roll. That innocent looking goody not only contains sugars, it is baked in one of many omega-6 oils such as soybean. Chips and fries are soaked in soybean oil; processed foods are manufactured with omega-6 oils for longer shelf life. While omega-6’s are essential -they are part of every cell membrane controlling what goes in and out of the cell — they must be in the correct balance with omega-3’s. If the balance shifts by consuming excessive omega-6, the cell membrane produces chemicals called cytokines that directly cause inflammation. Today’s mainstream American diet has produced an extreme imbalance of these two fats. The ratio of imbalance ranges from 15:1 to as high as 30:1 in favor of omega-6. That’s a tremendous amount of cytokines causing inflammation. In today’s food environment, a 3:1 ratio would be optimal and healthy. To make matters worse, the excess weight you are carrying from eating these foods creates overloaded fat cells that pour out large quantities of pro-inflammatory chemicals that add to the injury caused by having high blood sugar. The process that began with a sweet roll turns into a vicious cycle over time that creates heart disease, high blood pressure, diabetes and finally, Alzheimer’s disease, as the inflammatory process continues unabated. There is no escaping the fact that the more we consume prepared and processed foods, the more we trip the inflammation switch little by little each day. The human body cannot process, nor was it designed to consume, foods packed with sugars and soaked in omega-6 oils. There is but one answer to quieting inflammation, and that is returning to foods closer to their natural state. To build muscle, eat more protein. Choose carbohydrates that are very complex such as colorful fruits and vegetables. Cut down on or eliminate inflammation- causing omega-6 fats like corn and soybean oil and the processed foods that are made from them. One tablespoon of corn oil contains 7,280 mg of omega-6; soybean contains 6,940 mg. Instead, use olive oil or butter from grass-fed beef. Animal fats contain less than 20% omega-6 and are much less likely to cause inflammation than the supposedly healthy oils labelled polyunsaturated. Forget the “science” that has been drummed into your head for decades. The science that saturated fat alone causes heart disease is non-existent. The science that saturated fat raises blood cholesterol is also very weak. Since we now know that cholesterol is not the cause of heart disease, the concern about saturated fat is even more absurd today. The cholesterol theory led to the no-fat, low-fat recommendations that in turn created the very foods now causing an epidemic of inflammation. Mainstream medicine made a terrible mistake when it advised people to avoid saturated fat in favor of foods high in omega-6 fats. We now have an epidemic of arterial inflammation leading to heart disease and other silent killers. What you can do is choose whole foods your grandmother served and not those your mom turned to as grocery store aisles filled with manufactured foods. By eliminating inflammatory foods and adding essential nutrients from fresh unprocessed food, you will reverse years of damage in your arteries and throughout your body from consuming the typical American diet. Dr. Dwight Lundell is the past Chief of Staff and Chief of Surgery at Banner Heart Hospital , Mesa , AZ. His private practice, Cardiac Care Center was in Mesa, AZ. Recently Dr. Lundell left surgery to focus on the nutritional treatment of heart disease. He is the founder of Healthy Humans Foundation that promotes human health with a focus on helping large corporations promote wellness. He is also the author of The Cure for Heart Disease and The Great Cholesterol Lie.

The new aircraft, known as the SR-72, is the unmanned successor to Lockheed’sSR-71 Blackbird, a twin-engine, two-seater,supersonic aircraftthat was developed in the 1960s. The company’s new spy plane will be able to fly twice as fast as the Blackbird and three times faster than current fighter jets, accelerating to Mach 6, which is six times thespeed of sound, or more than 3,500 mph (5,600 km/h).

“Hypersonic is the new stealth,” Lelandtold Reuters. “Your adversaries cannot hide or move their critical assets. They will be found. That becomes a game-changer.”

Furthermore, Lockheed is designing thespy planeusing existing technology, which could help the company develop a prototype in five or six years for under $1 billion, he added.

Lockheed is aiming to fly a missile to demonstrate the new technology as early as 2018, and Leland said operational SR-72s could be in service by 2030, according to Aviation Week, which was first to report on the new project.

“What we are doing is defining a missile that would have a small incremental cost to go athypersonic speed,” Leland told Reuters.

The SR-72 is being developed by Skunk Works, Lockheed’s California-based advanced research program that previously worked on the SR-71 Blackbird and the famed U-2 spy plane.

The hypersonic SR-72 will feature a two-phase propulsion system, which uses a basic jet turbine to accelerate the plane to Mach 3. Lockheed is collaborating with rocket and missile propulsion manufacturer Aerojet Rocketdyne to incorporate this turbine with an air-breathing, supersonic ramjet engine to propel the vehicle from standstill to Mach 6.

The new spy plane will build upon Lockheed’s previous experimental hypersonic programs, such as theHypersonic Technology Vehicle2, or HTV-2, which was developed as part of the Defense Advanced Research Projects Agency’s (DARPA’s) Falcon Project.

In 2011, the unmanned, arrow-shapedHTV-2 gliderreached Mach 20 and controlled itself for approximately three minutes, before crashing into the Pacific Ocean. During the flight, surface temperatures on the vehicle reached 3,500 degrees Fahrenheit (1,930 degrees Celsius), which is hotter than a blast furnace capable of melting steel.

The SR-72’s predecessor, the SR-71 Blackbird, could accelerate to Mach 3.3 (more than 2,200 mph, or 3,540 km/h) at an altitude of 80,000 feet (24,400 m). The Blackbird made its first flight in December 1964, and was flown by the U.S. Air Force until 1998. The two-seater aircraft was capable of outracing potential threats during reconnaissance missions, including being able to accelerate and out-fly surface-to-air missiles if it was detected.